Oxidative stress is known to be closely related to aging and various diseases. Particularly, oxidative stress is known to be closely related to autoimmune responses, and examples of diseases caused by oxidative stress include inflammatory reactions, such as asthma, allergy, atopy and nasitis.
As is known, respiratory disease patients show an imbalanced ratio of oxidants to antioxidants, and superoxide dismutase (SOD), a peroxide inhibitor, relieves respiratory diseases. It was also reported that antioxidants can be used to treat inflammatory reactions caused by oxidative stress. In addition, it is known that reactive oxygen species (ROS) cause immune system abnormalities and autoimmune diseases and increase the expression of interleukin-4 (IL-4) and interleukin-13 (IL-13).
Interleukin-4 and interleukin-13 are cytokines made by T-helper 2 cells (Th2 cells) and are very closely related to autoimmune diseases. In signaling of these interleukins, Janus-associated kinase (JAK), STATE, IRS 1/2, phosphoinositol-3 kinase (PI-3 kinase) and the like are involved and cause proinflammatory cytokines, including interleukin-1, interleukin-6, interleukin-8, interleukin-10, interleukin-12 and the like. In addition, interleukin-4 and interleukin-13 are involved in the expression of immunoglobulin IgE, MHC class II antigen, and cluster of differentiation (CD23) and the proliferation of B cells and are also closely related to the differentiation of T helper 2 cells.
Particularly, bronchial asthma is a chronic allergic inflammatory disease in bronchi. Bronchial asthma occurs when the bronchial airways have inflammation or the bronchi have an increased sensitivity to allergens. It also occurs when the airway muscles become thicker or swell.
Asthma is caused by external factors or internal factors. The external factors include atmospheric pollutants, various allergens and industrial particles. These asthma triggers produce IgE in immune responses, and the produced IgE clogs the nasal, skin and airway passages and binds to receptors on the surface of mast cells in various organs to cause inflammation. The internal factors include genetic factors. It is known that human chromosome 5, 32-adrenoreceptor gene and human chromosomes 11, 12, 14 and 16 are involved in the occurrence of asthma and the changes in these genes increase IgE and cause hypersensitivity.
In asthma symptoms, CD4+ T cells in the airway are controlled, and upon exposure to triggering allergens, airway inflammation occurs which is characterized by an increase in Th2 immune responses, the inhibition of Th1 immune responses and the infiltration of eosinophils. Thus, various inflammatory cells, including eosinophils, neutrophils and lymphocytes, infiltrate bronchial mucosa and alveoli, and the kind and amount of cytokine secreted change. Therapies for controlling immune responses in bronchial asthma include avoidance therapy for allergens, and desensitization therapy for allergies, but it is actually impossible to avoid allergens.
Also, existing desensitization therapies that use steroids, β2-agonists and cromones are limited to patients with atopic bronchial asthma caused by some allergens and can cause serious adverse effects such as anaphylaxis. In addition, the development of asthma therapeutic agents, such as soluble IL-4 receptors and soluble IL-13 and anti-IL-5 antibodies, which use mechanisms for inhibiting the action of Th2-type cytokines, is in progress. However, many agents for treating asthma are available only on a physician's prescription and are mostly steroidal drugs which can cause adverse effects upon long-term use.
Accordingly, the present inventors have made extensive efforts to develop a pharmaceutical composition or food effective for the treatment of inflammatory, allergic or asthma disease, which is based on a food readily available to anyone and does not cause side effect even upon long-term use. As a result, the present inventors have found that an extract of paprika is effective for the treatment of the above disease, thereby completing the present invention.